ORIGINAL ARTICLE

Myocardial function and aerobic fitness in adolescent females

Thomas Rowland • Viswanath Unnithan •

Denise Roche • Max Garrard • Kathyryn Holloway •

Simon Marwood

Received: 24 October 2010 / Accepted: 7 January 2011 / Published online: 20 January 2011

� Springer-Verlag 2011

Abstract A recent report indicated that variations in

myocardial functional (systolic and diastolic) responses to

exercise do not contribute to inter-individual differences in

aerobic fitness (peak VO2) among young males. This study

was designed to investigate the same question among

adolescent females. Thirteen highly fit adolescent football

(soccer) players (peak VO2 43.5 ± 3.4 ml kg-1 min-1)

and nine untrained girls (peak VO2 36.0 ± 5.1 ml kg-1

min-1) matched for age underwent a progressive cycle

exercise test to exhaustion. Cardiac variables were mea-

sured by standard echocardiographic techniques. Maximal

stroke index was greater in the high-fit group (50 ± 5 vs.

41 ± 4 ml m-2), but no significant group differences were

observed in maximal heart rate or arterial venous oxygen

difference. Increases in markers of both systolic (ejection

rate, tissue Doppler S0) and diastolic (tissue Doppler E0,mitral E velocity) myocardial functions at rest and during

the acute bout of exercise were similar in the two groups.

This study suggests that among healthy adolescent females,

like young males, myocardial systolic and diastolic

functional capacities do not contribute to inter-individual

variability in physiologic aerobic fitness.

Keywords Peak oxygen uptake � Echocardiography �Cardiac output

Introduction

The greatest rate that oxygen can be delivered to and uti-

lized by exercising muscle (maximal aerobic power, peak

VO2) serves as the primary marker of physiologic aerobic

fitness as well as an index of performance capacity in

endurance exercise. The determinant factors which define

peak VO2 and explain inter-individual differences in aer-

obic fitness have been well defined in young males

(Rowland et al. 1999a, b; Obert et al. 2005). Level of peak

VO2 in this group is dictated specifically by the ability to

generate stroke volume at maximal exercise, which in turn

is a reflection of left ventricular end-diastolic and systolic

volume. On the other hand, variations in myocardial

function, defined as contractile rate and force (systolic) and

properties of relaxation (diastolic), appear to play no role in

defining maximal stroke volume, and, by extension, peak

VO2 among healthy young males (Rowland et al. 2009).

This is consistent with a model whereby peripheral, non-

cardiac factors such as the influence of plasma volume on

ventricular size play principal roles in defining level of

aerobic fitness (Perrault and Turcotte 1993).

Whether similar determinants influence variations in

aerobic fitness among young females has not been well

investigated. Certain information suggests that gender

differences might, in fact, exist. Stroke volume is lower in

female compared to male youths, even when body com-

position is considered (Rowland et al. 2000). In addition,

Communicated by Keith Phillip George.

T. Rowland (&)

Department of Pediatrics, Baystate Medical Center, Springfield,

MA 01106, USA

e-mail: thomas.rowland@bhs.org

V. Unnithan � D. Roche � M. Garrard � K. Holloway �S. Marwood

Sport and Exercise Physiology Research Team,

Liverpool Hope University, Liverpool, UK

Present Address:V. Unnithan

Centre for Sports, Health and Exercise, Staffordshire University,

Stoke-on-Trent, UK

123

Eur J Appl Physiol (2011) 111:1991–1997

DOI 10.1007/s00421-011-1835-1

athletically trained college-aged females demonstrate less

relative myocardial hypertrophy than their male counter-

parts (George et al. 1995). Compared to females, adult men

demonstrate a greater ventricular contractile response to

exercise (Higginbotham et al. 1984). In rats, myocardial

function with sympathetic stimulation is greater in males

than females (Vizgirda et al. 2002). Such gender differ-

ences could reflect differential effects of testosterone and

estrogen on myocardial function (Schaible et al. 1984;

Vuolteenaho and Ruskoaho 2003).

Among 10–11-year-old girls and boys, Obert et al.

(2005) found that resting values of left ventricular dimen-

sions and stroke volume served to differentiate VO2max

levels in low, moderate, and high-fit groups. Thoren and

Asano (1984) found greater maximal stroke volume but not

heart rate or arterial venous oxygen difference in a small

number of high-fit girls compared to low-fit subjects. The

role of myocardial systolic and diastolic functional

responses to exercise in differentiating levels of aerobic

fitness in young females has not previously been studied.

This study utilized echocardiographic techniques to

identify the determinant cardiac factors which define level

of peak VO2 in adolescent females. Specifically, attention

was focused on the potential role of myocardial systolic

and diastolic function in discriminating inter-individual

levels of aerobic fitness in this group.

Methods

Thirteen adolescent female football (soccer) players (mean

age 14.6 ± 0.7 years) and nine healthy, nonathletic girls

(15.0 ± 0.6 years) from a local school were recruited for

exercise testing. All were in good health, nonobese, non-

smokers, and taking no medications that would influence

cardiovascular fitness. No subject had taken oral contra-

ceptives. Data in the nonathletes were included in a

previously published study examining gender influences

on myocardial functional responses to acute exercise

(Rowland et al. 2010).

The footballers were participants in a competitive club,

with a training history averaging 10.3 ± 1.4 months per

year for the past 6.4 ± 0.9 years. By questionnaire, the

nonathletic group reported neither regular physical activity

nor participation in sports play. Level of sexual maturation

was estimated by Tanner stage self-assessment. Among the

soccer players, three were in stage 5, four in stage 4, three

in stage 3, one in stage 2, and one in stage 1. In the non-

athletic group, eight were in stage 4 and one in stage 3.

This study was approved by an institutional ethics

committee at Liverpool Hope University. Informed written

permission and assent were obtained from the parents and

subjects, respectively.

Stature and body mass were determined by stadiometer

and balanced beam scale, respectively. Body fat content

was estimated by the air displacement plethysmography

method (Bod Pod, Life Measurement, Inc., Concord, CA,

USA).

Left ventricular dimensions were measured at rest by

two-dimension directed M-mode echocardiography with

the subjects in the supine left lateral position (Model

HD11, Philips Medical Systems, Eindhoven, the Nether-

lands). Values were averaged from three measurements

made in the parasternal view, just distal to the tips of the

open mitral valve leaflets. Left ventricular end-diastolic

dimension (LVED) was recorded from the trailing edge of

the ventricular septum to the endocardial surface of the

posterior wall, coincident with the onset of the QRS

complex on the electrocardiogram. Ventricular septal and

posterior wall thicknesses were determined in end diastole.

Left ventricular end-systolic dimension (LVES) was mea-

sured as the shortest distance between the posterior edge of

the ventricular septum and posterior wall endocardium

during ventricular systole. Values of chamber dimensions

and wall thickness were expressed relative to the square

root of body surface area (BSA) (Gutgesell and Rembold

1990). Left ventricular fractional shortening (FS) was

calculated as (LVED – LVES)/LVED 9 100.

Left ventricular diastolic volume (LVEDV) was calcu-

lated by the formula of Teichholz et al. (1976): LVEDV

(ml) = [7(2.4 ? LVED)] 9 LVED3. Left ventricular

mass (LVM) was obtained by the cube formula 1.04

[(LVED ? LVPW ? LVS)3 – LVED3] – 14 (Devereux

and Reichek 1977). Both LVEDV and LVM were

expressed relative to BSA1.5 (Gutgesell and Rembold

1990).

Subjects performed a progressive maximal cycle exer-

cise test to exhaustion on an electronically braked ergom-

eter (Excalibur Sport 925900; Lode, Groningen, the

Netherlands). Cadence was maintained at 60 rpm with

initial and incremental loads of 35 W applied in 3-min

stages. Peak exercise was defined as the point when the

subject could no longer maintain the pedal cadence despite

verbal encouragement, in conjunction with objective evi-

dence of fatigue plus peak heart rate [180 bpm or RER-

max (peak respiratory exchange ratio)[1.00. No effort was

made to consider timing of menstrual period with sched-

uling of exercise testing.

Gas exchange variables were obtained using standard

open circuit techniques with a Cosmed K4b2 system

(Cosmed, Rome, Italy). A pneumotachometer was utilized

for recording minute ventilation. The system was calibrated

before testing with known oxygen and carbon dioxide

concentrations. Peak VO2 was defined as the average of the

two highest 20-s mean values determined during the final

minute of exercise.

1992 Eur J Appl Physiol (2011) 111:1991–1997

123

Heart rate was determined electrocardiographically.

Stroke volume was estimated at rest, during each sub-

maximal stage, and at peak exercise by standard Doppler

ultrasound techniques (Rowland and Obert 2002). A 1.9-

mHz transducer interrogated velocity of blood flow in the

ascending aorta from the suprasternal notch. The average

of the 3–5 highest velocity–time integrals (VTI) was

multiplied by the aortic valve area to obtain stroke volume

(SV). Aortic valve area was calculated from the maximal

aortic valve diameter at the valve hinge points measured at

rest in a parasternal long axis view with the subject in the

sitting position on the cycle ergometer. Acceptable validity

and reliability of this technique measuring stroke volume

have previously been reported (see Rowland and Obert

2002 for review).

Cardiac output (Q) was calculated as the product of

concomitantly obtained values of heart rate and stroke vol-

ume. Both Q and SV were indexed to body surface area.

Arterial venous oxygen difference was calculated as VO2/Q.

Arterial blood pressure was recorded in the left arm by

the auscultatory technique. Mean arterial pressure (MAP)

was calculated as MAP = 1/3(systolic – diastolic) ? dia-

stolic pressure. Systemic vascular resistance was derived

from MAP/Q.

Peak blood flow velocity across the mitral valve in early

diastole (E wave) was recorded by Doppler pulse wave

interrogation with 5.0 MHz transducer at the level of the

tips of the open valve leaflets in the apical four-chamber

view. Mean value was calculated as the average of the

consistently highest values (typically 3–10 beats). Late

diastolic filling velocity (A wave) was not considered as

this wave rapidly merged with the E wave with low-exer-

cise intensities.

Pulse-wave tissue Doppler imaging (TDI) was performed

at the lateral aspect of the mitral valve annulus to record

longitudinal myocardial systolic (S0 wave) and diastolic (E0

wave) velocities with the same transducer in the apical four-

chamber view. Each off-line measurement again represented

the average of the 3–10 highest velocities. Transducer

alignment was considered optimal when the ventricular

septum was observed to be vertical. To facilitate measure-

ments, one staff member positioned the transducer while the

other regulated the echocardiographic controls. All mea-

surements were made during spontaneous respirations.

Values for TDI-E0 and TDI-S0, both being influenced by

ventricular dimensions, were adjusted for LVED (Eidem

et al. 2004; Batterham et al. 2008). Satisfactory reliability of

this method during maximal exercise testing has been

reported previously, with coefficients of variation ranging

from 2.8 to 8.1% at maximal exercise (Bougault et al. 2008;

Rowland and Willers 2010).

The battery of measurements of heart rate, blood pres-

sure, VTI, mitral E, TDI-S0, and TDI-E0 were obtained at

rest, beginning at 1:30 in each 3-min stage, and during the

final minute of exercise. Systolic ejection rate, normalized

for left ventricular mass, and TDI-S0 were considered as

markers of systolic function (Bach 1996; Pai et al. 1991;

Roberson and Cui 2009). The former was calculated as

absolute stroke volume divided by systolic ejection time,

obtained from the duration of the VTI curve. Peak mitral

E velocity was interpreted as an indicator of the transmitral

pressure gradient, with TDI-E0 serving as a marker of

‘‘downstream’’ rate of myocardial relaxation (diastolic

function) (Jacques et al. 2004; Sohn et al. 1997) and the

ratio of E/E0 as an indicator of upstream left ventricular

filling pressure (Nagueh et al. 1997; Ommen et al. 2000)

(see Rowland (2008) for review).

Statistical analysis was performed with SPSS version 16

(SPSS Inc, Chicago, IL, USA). Values were expressed as

mean ± standard deviation. Values at rest and peak exer-

cise between the two groups were compared by indepen-

dent t test. Two-way ANOVA (group 9 time) with

repeated measures was used to examine the significance of

changes in variables during exercise. Post hoc comparisons

were made by Bonferroni-corrected t tests. Statistical sig-

nificance was defined as P B 0.05.

Results

Mean body mass for the athletes was 57.4 ± 8.0 kg, height

161 ± 5 cm, and body surface area (BSA) 1.59 ±

0.12 m2. Respective values for the nonathletes were

52.3 ± 7.0 kg, 160 ± 4 cm, and 1.53 ± 0.11 m2. Average

percent body fat was 16.3 ± 5.3% for the athletes and

20.1 ± 5.8% for the nonathletes (P [ 0.05 for all anthro-

pometric group comparisons).

No significant differences were observed in peak heart

rate between the athletes and nonathletes (189 ± 12 and

191 ± 9 bpm, respectively) or RER (1.01 ± 0.06 and

1.07 ± 0.07, respectively), indicating that both groups

performed to an equal maximal voluntary effort. Peak VO2

relative to body mass was 21% greater in the athletes

(43.5 ± 3.4 vs. 36.0 ± 5.1 ml kg min-1) (P \ 0.05).

Values for echocardiographic measurements at rest of

left ventricular size, wall thickness, contractility, mass, and

volume are presented in Table 1. The athletes demon-

strated a significantly greater average relative cardiac mass

as well as septal and posterior wall thicknesses. Ventricular

volume was greater in the athletes, but the difference from

nonathletes did not reach a level of statistical significance.

Global systolic function at rest, as indicated by values of

ventricular shortening fraction, was similar in the two

groups.

Cardiovascular variables at rest and maximal exercise

are outlined in Table 2. Maximal cardiac index was

Eur J Appl Physiol (2011) 111:1991–1997 1993

123

significantly greater in the athletes, a reflection of higher

relative stroke volume both at rest (?19%) and maximal

exercise (?25%). These variables accounted for the sig-

nificant inter-group differences in peak VO2, since maximal

values for arterial venous oxygen difference and heart rate

were similar in the athletes and nonathletes. Calculated

systemic vascular resistance was lower in the athletes both

at rest and maximal exercise, but no difference in the

magnitude of change during the exercise test was observed

between the two groups.

The pattern of stroke volume response to progressive

exercise in the athletes mimicked that of the nonathletes

(Fig. 1). At onset of upright exercise, values rose, but by

early-mid work intensities SV (\50% peak VO2) showed

no significant change to exhaustion. Values for stroke

index were greater for the athletes at all levels of exercise.

No significant differences were observed between the

athletes and nonathletes in resting or maximal values of

systolic function (Figs. 2, 3, 4). Adjusted systolic ejection

rate rose by 93 and 80% in the athletes and nonathletes,

respectively, and adjusted TDI-S0 by 121 and 148%. Simi-

larly, resting and exercise measures of diastolic function

were similar in the two groups. Adjusted TDI-E0 increased

by 122% in the athletes and 131% in the nonathletes, while

E/E0 remained stable in both groups of subjects. Repeated

measures ANOVA revealed main effects for exercise dura-

tion for all measures except E/E0 with group effects for Q and

SV. No group 9 time interaction was seen for any exercise

variable.

Discussion

The cardiac dynamics during a progressive upright exercise

test in healthy, untrained subjects are well recognized

(Rowland 2005). Following an early rise, stroke volume

shows little change at mid- and high-exercise intensities,

while left ventricular end-diastolic dimension, reflecting

ventricular preload, remains stable or declines slightly.

Markers of myocardial systolic and diastolic function

steadily rise, serving to maintain (rather than increase)

stroke volume as ventricular ejection and filling times

shorten with the increase in heart rate.

The findings in this study indicate that, within this

construct, myocardial functional capacity does not con-

tribute to inter-individual differences in aerobic fitness

(peak VO2) between average and high-fit adolescent

females. Despite a 21% difference in peak VO2, measures

Table 1 Resting echocardiographic measures of left ventricular

mass, volume, and dimensions in young female athletes (N = 13) and

nonathletes (N = 9)

Athletes Nonathletes

LVED (mm BSA-0.5) 37.1 ± 1.8 36.6 ± 1.7

LVES (mm BSA-0.5) 22.7 ± 1.9 22.5 ± 0.9

VSd (mm BSA-0.5) 7.2 ± 0.8 6.5 ± 0.7*

PWd (mm BSA-0.5) 7.3 ± 1.0 6.3 ± 0.5*

Shortening fraction (%) 38.8 ± 5.1 38.5 ± 2.0

LVEDV (ml BSA-1.5) 63.9 ± 7.1 61.1 ± 6.9

LVM (g BSA-1.5) 80.3 ± 11.9 63.7 ± 6.7*

Values are mean ± SD

LVED left ventricular end-diastolic dimension; LVES left ventricular

end-systolic dimension; VSd ventricular septal thickness, diastole;

PWd left ventricular posterior wall thickness, diastole; BSA body

surface area (m2)

* P B 0.05 for athletes versus nonathletes

Table 2 Cardiovascular measures at rest and maximal exercise in

athletes and nonathletes

Athletes Nonathletes

Heart rate (bpm)

Rest 73 ± 13 76 ± 14

Maximum 189 ± 12 191 ± 9

Stroke index (ml m-2)

Rest 42 ± 10 33 ± 6*

Maximum 50 ± 5 41 ± 4*

Cardiac index (L min-1 m-2)

Rest 3.02 ± 0.91 2.55 ± 0.72

Maximum 9.53 ± 0.99 7.80 ± 1.03*

Arterial venous oxygen difference (ml 100 ml-1)

Rest 7.5 ± 2.5 7.4 ± 2.1

Maximum 18.1 ± 2.7 17.6 ± 3.1

Systemic vascular resistance (units)

Rest 18.3 ± 4.9 23.0 ± 6.9*

Maximum 5.7 ± 0.7 7.4 ± 1.5*

Systolic function

Systolic ejection rate, adjusted (ml s-1 g-1 9 10-4)

Rest 19.9 ± 4.1 21.1 ± 4.2

Maximum 38.5 ± 6.3 37.9 ± 4.9

TDI-S, adjusted (cm s-1 mm-1 9 10-2)

Rest 18.0 ± 4.0 16.6 ± 3.2

Maximum 39.7 ± 6.7 41.2 ± 5.4

Diastolic function

Mitral E (cm s-1)

Rest 74 ± 13 75 ± 18

Maximum 151 ± 16 156 ± 19

TDI-E0, adjusted (cm s-1 mm-1)

Rest 0.27 ± 0.05 0.26 ± 0.05

Maximum 0.60 ± 0.06 0.60 ± 0.05

E/E0 adjusted

Rest 284 ± 52 297 ± 101

Maximum 251 ± 23 263 ± 36

Values are mean ± SD

* P B 0.05 athletes versus nonathletes

1994 Eur J Appl Physiol (2011) 111:1991–1997

123

of systolic and diastolic function were similar at rest and

during a progressive cycle test to exhaustion between these

two groups. Systolic ejection rate and TDI-S0, markers of

myocardial contractility, were similar at rest and rose by a

factor of approximately 2.0 in athletes and nonathletes.

Parallel improvements were observed in ventricular relax-

ation as indicated by a similar decline in TDI-E0 and a

stable E/E0 in both groups. These results mimic findings

previous reported in adolescent males (Rowland et al.

2009), supporting the conclusion that gender does not

influence the mechanistic determinants of physiologic

aerobic fitness in this age group.

Among the candidates offered by the Fick equation, the

variation in peak VO2 in the two groups of subjects was

dictated entirely by maximal stroke volume as average

values of heart rate and arterial venous oxygen difference

at maximal exercise were similar in the high- and average-

fit subjects. Then, by extension, these findings support a

model by which the increases in both myocardial con-

tractility and relaxation that normally occur during an acute

bout of progressive exercise do not serve to augment stroke

volume. This is clearly evidenced by the constant values of

stroke volume observed after the initial stages of such a test

that occur concomitant with significant rise in markers of

both systolic and diastolic functions. The effect of such

increases in myocardial performance therefore appears to

reflect the necessity for maintaining—rather than increas-

ing—stroke volume as systolic ejection and diastolic filling

periods progressively fall with increasing heart rate.

Further evidence of equality of ventricular performance

during progressive exercise in the two fitness groups

comes from the similarity observed in their patterns of

stroke volume response. In both, stroke volume ‘‘platea-

ued,’’ or remained stable after early work loads up to

exhaustion. The stroke volume curve was seen, in effect,

to be simply displaced superiorly in the high-fit subjects.

This stability of stroke volume, as noted above, is main-

tained by increasing ventricular systolic and diastolic

function as work load rises. Any exaggerated increases in

systolic and/or diastolic function, or greater functional

responses in one group compared to the other, would

35 70 105 140 175 210R25

35

45

55

65AthletesNonathletes

Power (W)

Str

oke

ind

ex (

mL

⋅m-2

)

Fig. 1 Stroke volume responses to progressive exercise in adolescent

athletes and nonathletes (mean ± SEM). Dashed line connects to

average maximal values. P \ 0.05 for all group comparisons

35 70 105 140 175 210R60

80

100

120

140

160

AthletesNon-athletes

Power (W)

Mit

ral

E (

cm⋅s

-1)

Fig. 2 Trans-mitral peak diastolic flow velocity (E wave) at rest and

during exercise

35 70 105 140 175 210R0.0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9AthletesNon-athletes

TD

I-E a

dj (c

m⋅ s

-1⋅ m

m-1

)

Power (W)

Fig. 3 Tissue Doppler E0 velocities at rest and during exercise

(values adjusted for left ventricular end-diastolic dimension)

35 70 105 140 175 210R150

200

250

300

350 AthletesNon-athletes

Power (W)

E /E

'ad

j

Fig. 4 E/E0 (adjusted) values for athletes and nonathletes at rest and

during exercise

Eur J Appl Physiol (2011) 111:1991–1997 1995

123

cause the stroke volume curve to rise during the course of

progressive exercise. Conversely, if myocardial functional

responses were impaired, the SV curve would fall with

increasing work loads. For example, the former pattern

has been suggested to occur in highly trained endurance

athletes (Gledhill et al. 1994), while the latter is observed

in patients with chronic heart disease (Rowland et al.

1999a, b).

Aerobic fitness is frequently considered as ‘‘cardiovas-

cular fitness’’ since individuals with higher levels of peak

VO2 are characterized by a greater capacity to generate

cardiac output. This feature, as indicated by the present

study and other reports, is a direct reflection of maximal

stroke volume. Inter-individual variations in maximal

stroke volume—the key element in aerobic fitness—are

not, however, related to any differences in heart muscle

performance. Instead, ‘‘cardiovascular fitness’’ is an

expression of non-cardiac factors, particularly increases in

plasma volume, which effect a greater ventricular end-

diastolic volume (Convertino 1991; Perrault and Turcotte

1993). Then the differences in aerobic fitness between

individuals might best be considered as a reflection of

variations in volume expansion of the cardiovascular sys-

tem rather than cardiac pumping capacity. Other factors

may play a role as well, including variations in peripheral

vascular conductance (Roche et al. 2010), and parasym-

pathetic-induced resting bradycardia (Perrault and Turcotte

1993).

The findings in the present study are consistent with the

above model but do not permit an analysis of contribution

to aerobic fitness of these extra-cardiac factors. Left ven-

tricular volume was not measured during exercise. Resting

values of left ventricular volume were greater in the high-

fit group, but group differences did not reach statistical

significance. This may be explainable by the small number

of subjects, a conclusion supported by the study of Obert

et al. (2005). These authors found that among 142 10-year-

old boys and girls, level of aerobic fitness (peak VO2) was

associated with resting values of stroke volume as well as

left ventricular chamber dimensions. In that study, resting

measures of systolic and diastolic functions did neither

emerge as predictors of VO2max, nor did systemic vascular

resistance. Unfortunately, information regarding the role of

variations in plasma volume on aerobic fitness is not

available in youth, reflecting methodological ethical

constraints.

Certain limitations of this study need to be recognized.

The number of subjects is low. Comparison of cardiac

responses to exercise was performed between high fit and

moderately fit groups, with similar levels of sexual matu-

ration, and thus the full spectrum of fitness in the healthy

adolescent population was not sampled. Previous studies of

cardiac findings involving high- and low-fit youth suggest,

however, that the findings in this study can be expected to

extend to all levels of fitness in adolescent females (Thoren

and Asano 1984; Rowland et al. 1999a, b; Obert et al.

2005). Further investigations using a broader range of fit-

ness, including responses to aerobic training and relation-

ships of variables to level of sexual maturation, are

warranted. Assessment of myocardial function in this study

did not involve all possible measures (intrinsic contractil-

ity, strain, rotation, twist, etc.), which will need to be

included in future investigations. The true mean arterial

pressure at high exercise intensities may not be accurately

estimated by the equation utilized in this study.

In summary, this study of adolescent females confirms

that (1) myocardial performance (systolic and diastolic

function) increases during an acute bout of progressive

exercise while stroke volume remains stable, (2) the

qualitative and quantitative aspects of these responses are

independent of levels of peak VO2, and, therefore, (3)

ventricular systolic and diastolic functional capacity does

not contribute to the factors which determine inter-indi-

vidual variations in aerobic fitness. Moreover, based on a

comparison with previous research data, these features

appear to be similar in young females and males.

Acknowledgments The authors are indebted to Philips Health Care

Ultrasound Division, Surrey, UK, and Gillian Nash and Julie Sand-

oval for their kind assistance in this study.

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